Lobar torsion following thoraco-abdominal oesophagogastrectomy

Following thoraco-abdominal oesophagogastrectomy for an adenocarcinoma of the lower oesophagus, an 81-year-old female with no pre-existing respiratory disease could not be weaned from mechanical ventilation. Right upper and middle lobe torsion were found at thoracotomy on the 14th postoperative day. Both lobes were resected. The patient was discharged from hospital after several postoperative complications. Pulmonary torsion is a rare, potentially life-threatening complication of thoraco-abdominal oesophagogastrectomy. Differentiation from the more common postoesophagectomy pulmonary complications can be difficult. Early post-thoracotomy lung opacification, in the absence of the expected degree of hypoxaemia, should trigger a suspicion of pulmonary torsion.     

Differential Regulation of RGS-2 by Constant and Oscillating PTH Concentrations

PTH has diverse effects on bone metabolism: anabolic when given intermittently, catabolic when given continuously. The cellular mechanisms underlying the varying target cell response are not clear yet. PTH induces RGS-2, a member of the Regulator of G-protein Signaling protein family, via cAMP/PKA, and inactivates PKC-mediated signaling. To investigate intracellular signaling pathways with different PTH concentration-time patterns, we treated UMR 106-01 osteoblast-like cells in a perfusion system. PTH was administered intermittently (4 min/h, 10⁻⁷ M) or continuously at an equivalent cumulative dose (6.6 × 10⁻⁹ M). cAMP was measured using radioimmunoassay, mRNA levels using real-time rtPCR and ribonuclease protection assay, and protein levels using Western immunoblotting. A single PTH pulse transiently increased cAMP levels by 2000% ± 1200%. In contrast to continuous PTH exposure, cAMP induction remained unchanged with intermittent PTH, ruling out desensitization of the PTH receptor. In continuously perfused cells, RGS-2 abundance was three to five times higher than in cells intermittently exposed to PTH for up to 12 h. MKP-1 and -3 were significantly less induced with pulsatile PTH; exposure-mode-dependent differences in MMP-13 and IGFBP-5 were small. Pulsatile but not continuous PTH administration prevents PTHrP receptor desensitization and accumulation of RGS-2 in osteoblasts, which should preserve PKC-dependent signaling.